The aim of the proposed research is to improve the understanding and treatment of human anxiety. Research conducted so far has suggested that similar nonhuman primate behaviors are elicited by dangerous situations, by electrical stimulation of the locus coeruleus (LC) noradrenergic system, or by chemical agents which activate the LC. These behaviors were blocked by agents which diminish the activity of the locus coeruleus on its efferent projections. Agents studied with this effect included several drugs with anxiolytic action in humans. In the opposite direction, chemical agents which increase LC activity increased the same behaviors and have been reported to induce anxiety in humans. On the basis of these and other data our hypothesis continues to be confirmed that alterations in LC activity are relevant to human anxiety and to the mode of action of anxiolytic drugs. Further studies of behaviors in monkeys are aimed at extending understanding of the neuronal mechanisms involved. Our methods include the use of pharmacologic agents with specific effects on LC activity, agents with known human anxiolytic activity, electrical stimulation and lesions of the locus coeruleus, and single unit activity recording from the LC in awake monkeys.